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Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

ABSTRACT: Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

PROVIDER: PRJNA1119399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29262390_1.fastq.gz	Fastqsanger.gz
	SRR29262390_2.fastq.gz	Fastqsanger.gz
	SRR29262391_1.fastq.gz	Fastqsanger.gz
	SRR29262391_2.fastq.gz	Fastqsanger.gz
	SRR29262392_1.fastq.gz	Fastqsanger.gz

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Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

Project description:Viruses have evolved diverse immune evasion strategies including targeting host pattern recognition receptors. The role of viral non-coding RNAs in modulating PRR activity is unclear. Here, we show that human cytomegalovirus (HCMV) produces long non-coding RNA4.9 that counteracts nuclear cyclic GMP-AMP synthase (cGAS)-mediated immune response to facilitate viral infection in primary human foreskin fibroblasts (HFFs). RNA4.9 interacts with host cGAS via its 75-nucleotide (nt) RNA region with predicted hairpin loops. Binding of RNA4.9 to cGAS inhibits cGAS enzymatic activity and downstream interferon response, and facilitates productive viral replication. Sterically blocking the folding of 75-nt region with antisense oligonucleotides during HCMV infection restores cGAS activity and impairs viral replication. We also found that the specific localization of RNA4.9, which concentrates near HCMV DNA, is correlated with its efficient binding to cGAS and subsequent immune suppression. Our findings demonstrate viral non-coding RNAs as critical cGAS regulators and potential therapeutic targets.

2025-06-11 | GSE268887 | GEO

Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

2025-06-12 | GSE270524 | GEO

Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

Project description:Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

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Project description:Human Cytomegalovirus long non-coding RNA counteracts nuclear cGAS to facilitate immune evasion

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β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion

Project description:Virus infection may induce excessive interferon (IFN) responses that can lead to host tissue injury or even death. β-arrestin 2 regulates multiple cellular events through the G protein-coupled receptor (GPCR) signaling pathways. Here we demonstrate that β-arrestin 2 also promotes virus-induced production of IFN-β and clearance of viruses in macrophages. β-arrestin 2 interacts with cyclic GMP-AMP synthase (cGAS) and increases the binding of dsDNA to cGAS to enhance cyclic GMP-AMP (cGAMP) production and the downstreatm stimulator of interferon genes (STING) and innate immune responses. Mechanistically, deacetylation of β-arrestin 2 at Lys171 facilitates the activation of the cGAS–STING signaling and the production of IFN-β. In vitro, viral infection induces the degradation of β-arrestin 2 to facilitate immune evasion, while a β-blocker, carvedilol, rescues β-arrestin 2 expression to maintain the antiviral immune response. Our results thus identify a viral immune-evasion pathway via the degradation of β-arrestin 2, and also hint that carvedilol, approved for treating heart failure, can potentially be repurposed as an antiviral drug candidate.

2020-10-22 | GSE159735 | GEO

An HIV protein mediates immune evasion by targeting cGAS–STING signaling

Project description:The cyclic GMP-AMP synthase (cGAS) recognizes Y-form cDNA of HIV-1 and initiate the antiviral immune response through cGAS–STING–TBK1–IRF3–type I IFN (IFN-I) signaling cascade. HIV-1 uses several strategies to interfere with the host immune molecules and mediate immune evasion. However, the potential role of HIV-1 proteins in cGAS–STING signaling remains unclear. Here we report that the HIV-1 protein p6 suppresses HIV-1-stimulated expression of IFN-I and promotes the immune evasion. Mechanistically, p6 bound with STING and inhibited the activation of STING and the interaction between STING and TBK1. Moreover, the glutamylation of p6 at Glu6 residue inhibited the interaction between STING and TRIM32 or AMFR, which subsequently suppressed the K27- and K63-linked polyubiquitination of STING at Lys337, therefore inhibited STING activation and type I IFN production, while the mutation of Glu6 residue lost the inhibitory effect. However, CoCl2, an agonist for cytosolic carboxypeptidases (CCPs), counteracted the glutamylation of Glu6 residue of p6 and promoted IFN-I production to block the immune evasion of HIV-1. These findings not only reveal a previously unknown mechanism through which an HIV-1 protein mediate immune evasion, but also provide a new therapeutic drug candidate to treat HIV-1 infection.

2021-11-25 | GSE189384 | GEO

An HIV protein mediates immune evasion by targeting cGAS–STING signaling

Project description:An HIV protein mediates immune evasion by targeting cGAS–STING signaling

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Centromeric DNA amplification triggered by viral proteins activates nuclear cGAS

Project description:The cGAS-cGAMP-STING pathway is crucial for antiviral immunity. While cytosolic cGAS detects viral DNA, most DNA viruses shield their genome and invade the nucleus, where chromatin restricts cGAS activation. How viruses may activate nuclear cGAS is not well understood. Here, we show that several herpesvirus proteins trigger nuclear cGAS activation by perturbing centromeres, where cGAS is enriched. The herpes simplex virus type 1 (HSV-1) ubiquitin ligase ICP0, which degrades centromeric proteins, promotes centromeric DNA amplification through the translesion DNA synthesis (TLS) pathway in quiescent monocyte-derived cells, thereby activating nuclear cGAS. During infection, HSV-1 evades this detection by also expressing UL36USP, a suppressor of TLS. Similarly to ICP0, the cytomegalovirus IE1 protein causes centromeric DNA amplification and cGAS activation. We define this mechanism as Viral-Induced Centromeric DNA Amplification and Recognition (VICAR), uncovering a non-mitotic, immune-activating role of centromeres.

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Gene induction in STAT1-/- fibroblasts transduced with lentiviruses expressing human cGAS

Project description:The hypothesis tested was that lentiviral driven cGAS expression activates antiviral gene expression. Cells were transduced with lentiviruses expressing cGAS or a control (firefly luciferase). Total RNA was harvested 48 h post-transduction and processed for Illumina BeadArray.

2013-12-01 | E-GEOD-52241 | biostudies-arrayexpress

The Acetyltransferase ARD1 Induces Glutathione Synthesis to Facilitate Ferroptosis Evasion in Hepatocellular Carcinoma

Project description:The Acetyltransferase ARD1 Induces Glutathione Synthesis to Facilitate Ferroptosis Evasion in Hepatocellular Carcinoma

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